{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T00:17:31Z","timestamp":1790727451686,"version":"4.1.0"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2002,5,1]],"date-time":"2002-05-01T00:00:00Z","timestamp":1020211200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2002,5,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>NF-\u03baB is a ubiquitously expressed transcription factor involved in the regulation of innate and adaptive immunity. As part of studies to define the role of various NF-\u03baB family members in Th cell development and maintenance, we infected NF-\u03baB2\u2212\/\u2212 and control mice with Leishmania major and followed disease progression. NF-\u03baB2\u2212\/\u2212 mice on a normally resistant background develop chronic nonhealing lesions associated with uncontrolled parasite replication and a failure to develop an IFN-\u03b3 response. We show that there are no intrinsic defects in Th cell differentiation in the absence of NF-\u03baB2. Indeed, NF-\u03baB2\u2212\/\u2212 T cells are able to develop a Th1 phenotype and protect recombination-activating gene\u2212\/\u2212 mice from progressive cutaneous leishmaniasis. We demonstrate instead that the susceptibility of NF-\u03baB2\u2212\/\u2212 mice to L. major is the result of an IL-12 deficiency, and we provide evidence for a specific impairment in CD40-induced IL-12 production by macrophages lacking this transcription factor.<\/jats:p>","DOI":"10.4049\/jimmunol.168.9.4406","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:46:54Z","timestamp":1398023214000},"page":"4406-4413","source":"Crossref","is-referenced-by-count":35,"title":["NF-\u03baB2 Is Required for Optimal CD40-Induced IL-12 Production but Dispensable for Th1 Cell Differentiation"],"prefix":"10.1093","volume":"168","author":[{"given":"Kendra","family":"Speirs","sequence":"first","affiliation":[{"name":"Department of Pathobiology, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge","family":"Caamano","sequence":"additional","affiliation":[{"name":"Medical Research Council Center for Immune Regulation, School of Medicine, University of Birmingham, Edgbaston , Birmingham ,","place":["United Kingdom"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael H","family":"Goldschmidt","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher A","family":"Hunter","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Phillip","family":"Scott","sequence":"additional","affiliation":[{"name":"Department of Pathobiology, University of Pennsylvania , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2002,5,1]]},"reference":[{"key":"2026020209044696100_R1","first-page":"225","volume-title":"Annu. 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